Staphylococci

Dr. Ng Woei Kean

Ph.D. (Molecular Medicine)
 General characteristics
• A gram positive organisms which is round in
shape (coccus), non-motile, non-spore forming
and catalase positive. It is arranged in clusters.
 The genus Staphylococcus is composed of 24
species some of them are pathogenic to human
or animals which includes:
S. aureus, S. epidermidis, S. saprophyticus,
S. hominis, S. hemolyticus, and S. warneri
Distinguishing characteristics of major species of
genus Staphyl ococcus

Properties S. S. S.
aureus epidermidis saprophyticus

Anaaerobic + + -
growth

Coagulase + - -

Alpha toxin + - -

Staphylococcus epidermidis
Mannitol + v S v R * It causes nosocomial infection.
Novobiocin S
sensiti vity Staphylococcus saprophyticus

*Causes 10-20% of primary Urinary

Tract Infections in young women (16-
35yo)

3
Features Found in Staphylococci and Other
Gram Positive Organisms
• A Cell Envelope composed of:
- thick peptidoglycan (PDG) layer (100-300Å)
- Plasma membrane
- Lipoteichoic acid
- Proteins can be excreted outside cell
- Some have teichoic acid
Features Found in All Staphylococci
• Gram-positive cocci that grow in clusters;
they can also be seen singly, or in pairs.
• Divide perpendicular to last plane of division.
• Catalase positive
• Facultative organisms
• Non motile
Catalase positive:
 Staphylococcus aureus
Features Found in Staphylococcus aureus
• Coagulase positive
• Thermostable nuclease positive
• High salt tolerance (7.5%-10%)
• Mannitol positive (i.e., Mannitol is fermented to
organic acids.). Phenol red indicator change to
yellow in acid pH
• Ribitol in their teichoic acid
• Often produce beta-haemolysis
Beta-haemolysis:
• Staphylococcus aureus is not normal flora, but it
transiently colonizes the nasopharynx anterior
nasal vestibules, skin and GIT & upper
respiratory tract.
• 25% adults are normally colonized with S.
aureus. 30% prolonged and 50% intermittent
careers of the organism.
• 20% people are never colonized.
• Increased chances of colonization in medical
personnel, diabetics, and IV drug users.
 Diseases caused by
Staphylococcus
1. Direct infection – skin
Folliculitis, Impetigo, carbuncle, abscess,
cellulitis, wound infection

Furuncle Impetigo Curbuncle

2. Deep infection
After trauma or surgery: Bursitis, athritis,
osteomyelitis, pneumonia, endocarditis.
Predisposing factors: old age/reduced host
defense/alcoholism/steroid/chemotoxic
therapy
3. Blood stream infection Bacteremia/ Sepsis
- with or without metastatic infection
- with or without vasculitis and coagulopathy
-with or without sepsis inflammatory
syndrome
4. Toxin mediated diseases
Food poisoning
Scalded skin syndrome
Toxic shock syndrome
Food poisoning
• Ingestion of Staphylococcus enterotoxin
contaminated food.
• Results in acute vomiting and diarrhea within 1-5
hours.
• Usually no fever and recovery is rapid
Scalded Skin Syndrome
• Results from exfoliatin in a Staphylococcus
lesion.
• Desquamation of epithelial sheets in all part of
the body.
• Widespread in neonates.
Toxic Shock Syndrome
• Toxic shock syndrome toxin (TSST-1) is the
major cause of Staph. Toxic shock.
• Different from enterotoxins
• Can stimulate the release of cytokines through
superantigen mechanism (exotoxin that interfere
with the immune response)
• May have direct toxic effects on endothelial
cells.
• Fever/vomiting/diarrhea/muscle pain followed by
shock/renal and hepatic injury.
Structure of S. aureus.
 Virulence factors of
Staphylococcus aureus
A) Binding Proteins and Capsules
1. Protein A
• 42 kilodalton protein covalently linked to
peptidoglycan; some is released extracellularly.
• Binds IgG by the Fc portion. Now IgG cannot
react with the Fc receptor on phagocytes ;
interfering with opsonisation.
2. Fibronectin, Fibrinogen, Vitronectin, and
Collagen type II binding proteins
• Mediate localization and adherence of the
organisms through binding extracellular matrix
proteins.
• Experiments showed that if collagen binding
protein genes were deleted, the ability to cause
arthritis in mice was greatly reduced.
3. Capsule (called - microcapsule)
• Types 5 and 8 account for 70% of all invaders
(11 types).
• Inhibits phagocytosis.
B) Enzymes
1. Clumping Factor (fibrinogen binding protein,
bound coagulase)
• It is a cell surface compound.
• When S. aureus is mixed with plasma, it forms
clumps because of an interaction between
fibrinogen and clumping factor.
• Clumping factor allows Staphylococcus aureus
to adhere to fibrinogen.
2. Coagulase
• Stimulates the conversion of fibrinogen to fibrin
by binding prothrombin. This complex becomes
active and initiates fibrin polymerization. This
process is not calcium dependent.
• Coated with fibrin, Staphylococcus aureus is
resistant to phagocytosis and the fibrin
deposition in an area contributes to localization
of the infection.
3. Staphylokinase
• Causes clot dissolution, activates conversion of
plasminogen to plasmin which is fibrinolytic.
• Staphylokinase is phage encoded.
4. Hyaluronidase
• Hydrolyzes hyaluronic acids that are present in
the extracellular matrix of connective tissue.

5. Lipase
• Helps Staphylococcus aureus to disseminate.
C) Toxins
1. Alpha Hemolysin
• It causes membrane damage by forming pores
in eukaryotic membranes.
• The channel size is pH dependent.
• Pore formation will hemolyzes RBCs, destroys
platelets, and kill WBCs by forming channels in
their membranes that causes a leak.
• Most potent of the S. aureus hemolysins.
2. Beta-hemolysin
• Toxic for monocytes, but not for PMNs,
fibroblasts or lymphocytes.
• Found in strains causing mastitis.
3. Panton-Valentine leukocidin
• Found in 5% of all S. aureus strains and in 50%
of ones from abscesses.
• Lethal to PMNs, disrupts their membranes
through pore formation which leads to increased
permeability.
• Sub-lytic concentrations of leukocidin cause
Leukotriene B4 (LTB4) release from PMNs and
increases IL-8 synthesis leading to inflammation.
4. Exfoliative exotoxin (ET)
• Exfoliatin causes intercellular splitting of the
epidermis between the stratum spinosum and
stratum granulosum, presumably by disruption
of intercellular junctions.
• Two antigenic variants of exfoliatin (ET-A and
ET-B) are antigenic in humans, and circulating
antibody confers immunity to their effects.
• Exfoliative exotoxin causes scalded skin
syndrome in newborns, and bullous Impetigo in
older kids and adults.
• The exfoliatin toxin causes extensive sloughing
of epidermis to produce burn like effects on the
patient.
5. Toxic shock syndrome toxin (TSST-1)
• TSST-1 is a 22 kilodalton peptide.
• Causes Toxic Shock Syndrome whose
symptoms include: fever, desquamative skin
rash, hypotension, multiple system involvement,
and potentially death.
• Absorbed toxin induces production of IL-1B and
tumor necrosis factor by monocytes.
6. Enterotoxin (SE)
• Types A-E (C has 3 subtypes)
• Heat stable (100 °C for 30 mins)
• Causes food poisoning. 1-6 hours post
ingestion, a patient has the following
symptoms: increased intestinal peristalsis,
vomiting, and diarrhea.
• Toxin appears to act on neural receptors in
upper GI tract leading to a stimulation of the
vomiting center.
 Laboratory Diagnosis
• One or more of the specimens should be
collected for demonstration of organisms by
gram staining or by culture.
• Pus from abscesses, wounds , burns ,etc.
• Feces or vomit or the remains of foods from
patient with suspected food poisoning.
• Blood from patients with suspected bacteremia
e.g. septic shock, osteomylitis,or endocarditis.
• Mid-stream urine from patients with cystitis or
pylonephritis.
• Anterior nasal swabs ( moistened in saline or
sterile water ) from suspected carriers.
• Sputum from cases of lower respiratory tract
infections such as postinfluenzal or ventilator
associated pneumonia.